Prostacyclin (PGI) is formed by the normal endothelium of some blood vessels (BV), (e.g., aorta) from prostaglandin endoperoxides (derived endogenously or perhaps exogenously). PGI is a short-acting, potent relaxer of vascular smooth muscle and inhibitor of platelet (P) aggregation (A). PGI may protect BV from uncontrolled PA and release, which may be linked to the genesis of atherosclerosis (AS) lesions, while still allowing for some P adhesion to occur (for maintenance of vessel integrity). Factors influencing PGI generation are thus important to examine in terms of AS and other pathophysiologic states involving P interactions with BV. Certain lipid peroxides (LP) (e.g. 15-hydroperoxyarachidonic acid; 15-HPAA) inhibit PGI generation by BV microsomes. Superoxide (SO) is an active oxygen species involved in intracellular reactions. SO can cause LP formation from membrane and plasma lipids. SO in blood is available from leukocytes and perhaps platelets. X-irradiation (which forms SO and other free radicals) increases PGI production by cultured endothelial cells. We find BV rings exposed to a low level SO generating system produce more PGI (measured by inhibition of PA). We propose to examine the finding in detail, using BV rings and cultured endothelial cells as PGI producers, and a combination of PA assay for PGI and radioimmunoassay for the PGI metabolite 6-keto-prostaglandin F1 alpha. Pharmacologic inhibitors of arachidonate conversion (dexamethasone, aspirin, tranylcypromine) and some specific biochemical agents (superoxide dismutase, catatase, radical traps) will be used to attempt to identify mechanism and stage of effect. Contrast and comparison with 15-HPAA and X-irradiation will also be done.